This year we have developed micro-sattelite markers for both the penguin(S. demersus) and for avian parasites that infect these creatures. We feel that the analysis of this parasite-host pair provides a wonderful oportunity to follow the distribution of related phenotypes of parasite and host over the years and the degree of association that they maintain. We have obtained collectionsof blood(avian blood cells are nucleated) collected every year since 1999 and are now in place to use the stored material to test samples from both isolated islands and penguins that have congregated outside their native habitat. One central question that is easily approached is whether parasites evolve with their local hosts(micro-evolution) as opposed to evolution being based at a species level. In other words is parasite diversity reflective of an isolated area or of the species as a whole. Establishing the concept here doesn't necessarily reflect that of a highly mobile human population but is reflective of the parasitic process.[unreadable] [unreadable] The shorter term impact of studying the threat posed by emerging parasites using avian malarias as a model; would be to explore the dynamic of emergent infectious diseases. Our model is Plasmodium juxtanucleare in S. demersus which we reported as an emerging disease three years ago. We will describe jointly the malarial parasites and host population structures and other aspects of their demographic histories; We will illustrate basic concepts of microevolution by using a single parasites and their host. The long-term broader impact will be the integration of cross-disciplinary approaches to explore host parasite relationships. We believe that understanding this interdisciplinary partnerships is a fundamental disease control. This proposal is our contribution to incorporate procedural, and cognitive levels of knowledge in population genetics into current research programs directed [unreadable] [unreadable] Plasmodium species face dramatic but predictable environmental changes during their life cycles, to which they must respond. These changes vary in degree and effect transmission of parasites and perhaps even the distribution of parasite populations. This includes predictable changes in temperature during transmission. As the fever cycle in humans illicit a defined response from the parasite so does the transmission of Plasmodium falciparum from human to mosquito which involves a temperature drop for the parasite. Both types of temperature drop signal the parasites cellular machinery and activates transcriptional change. We used micro-array analysis to monitor the transcriptional changes that are solely related to this temperature change. Expression of one gene was stimulated 135 fold by lowering the temperature of the asexual parasite from 37:C to 26:C. The transcript is a non-coding RNA whose gene is positioned immediately upstream of the S type ribosomal RNA genes but is under different control. Transcriptional change is initiated by temperature but the initial effects on the cells transcriptional machinery come from a cytoplasmic factor. A kinase is directly, but perhaps not solely, responsible. Inhibition of particular forms of kinase directly affect the transcription of the non-coding RNA described above The study has implications for understanding how the parasite senses and responds to environmental change.